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Hypernatraemia- Raised sodium

Sodium imbalances are encountered frequently in the community. While evaluating blood results in General Practice -this chart on A4Medicine can help clinicians formulate a management plan for patients with results suggesting hypernatremia or a raised Na level. Physiological response to a raised Na level is discussed to aid understanding followed with an emphasis on evaluation to ascertain the cause. With no clear guidelines on management, user is advised to take into account several factors as speed of onset, level, symptoms along with a clinical assessment to  make a management plan

Hypernatremia-Frequent electrolyte disorder in hospitalized patients Caused by loss of water or gain of sodium or both Hyperosmolar condition caused by ↓↓ TBW relative to electrolyte content Often marker of severe underlying disease and associated with very high mortality rates of 40-60 % Always associated with and ↑ ed effective plasma osmolality and hence with a reduced cell volume Relatively rare in community and seen less than hyponatraemia In community often seen in septic elderly people ( eg CVA , dementia ) 
○ ↑ sweating
○ reduced oral intake and reduced renal concentrating mechanisms 
( ie inadequate concentration of urine in face of restricted water intake )
○ limited access to water or an impaired thirst mechanism

Causes- hypovolaemic sodium deficit with a relatively greater water deficit-Renal Na loss Diuretic therapy Glycosuria ( HONK ) GI Na loss Colonic diarrhoe Skin Na loss Excessive sweating

Often in dehydrated patients with low water intake and high fluid loss. Euvolaemic-Diabetes insipidus

Excess loss of urinary free water.Hypervolaemic
Na retention with relatively less water retention.Enteral or parenteral feeding IV or salt administration Chronic renal failure
( during water restriction )

Often Iatrogenic

Mild 146-148 mmol/l ( if asymptomatic-statistical outlier) Moderate 149-154 ( Assess and investigate ) Severe > 155 ( detrimental – Admit )

Why is this important – Clinical approach to hypernatraemia is often challenging – underlying pathophysiology is complex It leads to diverse effects in multiple organ systems with a high mortality rate Under normal conditions – a state of normonatraemia is acheived by thirst driver water intake and arginine vasopressin ( AVP ) mediated water conservation in the kidney Hypernatraemi causes increased ECF osmolality and tonicity Increased plasma osmolality due to hypernatremia causes water to move out of brain cells causing cell shrinkage As the brain is particularly sensitive to changes in cell volume the symptoms are primarily neurological Physiological responses cause can an adaptive regulatory volume increase which imports ionic osmolytes ( Na , K and Cl- ) within minutes with water following suit Acute hypernatraemia , although rare if untreated can cause osmotic demyalination syndrome ( ODS ) and cerebral haemorrhage ( brain shrinkage can lead to vascular rupture and IC haemorrhage ) In chronic setting the brain volume is further normalized by uptake and synthesis of organic osmolytes like amino acids , polyols and methylamine

Clinical features-Often subtle and non specific in elderly Volume depletion -hypotension ( supine and/ or orthostatic ) Nausea and vomiting , diarrhoea Excessive sweating Concentrated scanty urine ( oliguria ) ↑ thirst , polyuria ( from diabetes insipidus ) Neurological symptoms -due to dehydration of neurons and brain shrinkage
○ altered mental state
○ irritability
○ weakness
○ neuromuscular irritability
○ focal neurological deficit
○ coma or seizures Increased risk of Subarachnoid haemorrhage or intracerebral bleeding

history-Assess rate of onset
○ if developed within last 48 hrs –> Acute ( more prominent symptoms )
○ over 48 hrs –> chronic ( can be asymptomatic ) Outside hospital setting patients generally
○ elderly and debilitated
○ often present with an inter-current ( febrile ) illness Determine reason why it could not be prevented
○ altered mental state
○ factors causing increased fluid secretion eg
 diabetes mellitus
 vomiting Diabetes insipidus- consider and explore symptoms and causes
 eg head trauma Medications ( Notably lithium ) Fluid intake Urine output

risk factors-Age ( infants and elderly ) Mental or physical impairment Uncontrolled diabetes ( solute diuresis ) Underlying polyuria disorders Diuretics Heart disease Bed-ridden Institutionalization – care home patients 10 times more likely to be dehydrated than patient who live in own home ( BMJ 2015 ) Hospitalization ( particularly ICU )

Differential diagnosis-Cirrhosis Hypocalcaemia Hyponatraemia Type 1 DM

Approach to hypernatremia –Repeat to confirm 
○ acute and changing
○ chronic and established

Changes up to 5 mmol/l can reflect non-significant variation
 Ascertain rate of onset Check thirst Assess fluid status – look for hypovolaemia Neurological state Exclude diabetes – control hyperglycaemia Stop diuretic- where relevant Control GI fluid loss Address Pyrexia Exclude Lithium toxicity

Investigations-Electrolytes ( Na , K , Calcium ) Glucose Urea Creatinine Urine electrolytes ( Na and K ) Urine and Plasma osmolality ( If diabetes insipidus suspected ) 24 hr urine volume Further investigations for Diabetes inspidus as
dynamic testing
desmopressin challenge
imaging to identify hypothalamic lesions.
Serum and urine osmolality are mentioned in literature as part of investigation for hypernatremia but these are not routinely requested in primary care setting

Urine osmolality is controlled by ADH and is used to detect the ratio of water and solutes in the urine. A high UrOs can indicate fluid losses ( e.g GI loss , diuretics ) and a low UrOs can indicate diabetes insipidus or water diuresis

Serum Osmolality can be used to check the hydration status. It measures the ratio of water and solutes in the serum.

Urinary Na conc can also help in diagnosis by indicating if the loss is renal or extra-renal

management- Presence or absence of symptoms Identification of underlying cause Correction of Volume status Correction of hypertonicity

 Admit if
○ Na > 155
○ Na 146-154 clinical cause not apparent and oral re-hydration is not possible in a dehydrated patient

If < 149- 154
○ check potassium , urea , Cr , Ca , Glu
○ r/o Lithium induced Nephrogenic diabetes insipidus
 Lithium toxicity
 Fluid therapy to correct hypernatraemia- in hospital Too rapid correction can lead to dangerous cerebral oedema – treatment should be slow and careful


  1. Evaluation of Renal Function, Water , Electrolytes , and Acid-Base Balance : Henry’s Clinical Diagnosis and Management by Laboratory Methods Twenty-Third Edition
  2. Diagnosis and treatment of hypernatraemia Best Practice and Research : Clinical Endocrinology and Metabolism , 2016-03-01 , Volume 30 , Issue 2 , Pages 189-203
  3. Hypernatraemia : aetiology and clinical assessment Davidson’s Principles and Practice of Medicine- Edited by Brian R Walker et al
  4. Seldin and Giebisch’s The Kidney , Fifth Edition
  5. Medscape : Hypernatraemia Ivo Lukitsch et al 2016
  6. Oxford Handbook of Geriatric Medicine-Hypernatraemia
  7. Prevalence , risk factors and prognosis of hypernatraemia during hospitilization in internal medicine The Netherlands Journal of Medicine December 2015 , Vol 73 , No 10
  8. Hyponatraemia and hypernatraemia : pitfalls in testing BMJ 2007 ; 334 :473
  9. Acid-base , fluids and electrolytes -Robert F . Relilly et al
  10. Hospital Physician ; Hypernatraemia Internal Medicine / Hospital Medicine Volume 14 , part 1
  11. Merck Manual Professional Edition : Hypernatraemia
  12. A primary care approach to sodium and potassium imbalance BPAC NZ via
  13. Hypernatremia: A systems-based approach
    Noto Joseph G, Bollu Ravindra, Sturzoiu Tudor, Nanda Sudip
    Year : 2018 | Volume:  4 | Issue Number:  3 | Page: 266-270;year=2018;volume=4;issue=3;spage=266;epage=270;aulast=Noto
  14. Management of hypernatraemia ABC of Intravenous Fuids , Electrolyte Disorders and AKI Management in Adults accessed via
  15. Hypernatremia Qi Qian



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